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Toxicity studies indicated that the mysid (Mysidopsis almyra) was more sensitive to the water-soluble fractions (WSFs) of No. 2 fuel oil than were either juvenile white shrimp (Penaeus setiferus) or juvenile brown shrimp (Penaeus aztecus) with 48 hour TLm values of 1.1, 1l8, and 2.9 ppm, respectively. The two refined oils, No. 2 fuel oil and Venezuelan bunker C, were generally >6 times more toxic to mysids than were either southern Louisiana crude or Kuwait crude. Postlarval brown shrimp were much more resistant to No. 2 fuel oil WSF than larger juveniles. Naphthalene compounds were determined by bioassay studies to be responsible for most of the toxicity of No. 2 fuel oil. Small juvenile brown shrimp accumulate less naphthalene (N), methylnaphthalenes (MN) and dimethylnaphthalenes (DMN) and depurate these compounds more slowly than do larger juveniles. The accumulation and release rates of N, MN and DMN for different size classes of brown shrimp has helped explain the greater sensitivity of larger brown shrimp to No. 2 fuel oil WSF compared to smaller shrimp. Brown shrimp selectively accumulate alkylnaphthalenes over other compounds when exposed to No. 2 fuel oil WSF, but these are depurated to background levels within 10 days. Most (80%) of the internal N, MN, and DMN accumulates in the digestive gland of brown shrimp after exposure to the WSFs of No. 2 fuel oil. In general, respiratory rate was not significantly different for adult mysids and various sizes of brown shrimp after exposure to concentrations of oil WSF, but was always altered (produced characteristic patterns of respiratory rate depression and stimulations) while these organisms were exposed to different concentrations of oil WSFs. Exceptions were noted when mysids were exposed to Kuwait SWF and oil-water dispersions of No. 2 fuel oil and when postlarval brown shrimp were exposed to the WSFs of No. 2 fuel oil after which respiratory rate was determined. The total concentration of naphthalene and alkylnaphthalenes in the WSF of No. 2 fuel oil, which caused a maximum respiratory response from mysids, was also present in the oil-water dispersion (OWD) which elicited the maximum respiratory response by these animals. Those brown shrimp which exhibited respiratory rates greater than controls were found to still contain significant amounts of N, MN, and DMN (26 hour) after exposure to oil. Growth rate and molting frequency were unaffected by both an initial high dose of No. 2 fuel oil WSF and periodic low doses of the WSFs of No. 2 fuel oil for a period of over 30 days. Exposure to No. 2 fuel oil did not affect the rate of stabilization of blood chloride ion concentrations after brown shrimp were transferred to salinities which were 10 o/oo higher and lower than the salinity to which they were previously acclimated. Greater blood chloride ion fluctuations were noted for oil exposed shrimp than for controls during the stabilization period after salinity shock. Excessive fluctuations were positively correlated with internal concentrations of N, MNs, and DMNs over a 96 hour period. After No. 2 fuel oil was poured over a shrimp mariculture pond, much of the oil became concentrated in the sediments. The N, MN, and DMN concentrations in white shrimp, oysters (Crassostrea virginica) and clams (Rangia cuneata) reached an equilibrium with concentrations in the sea water phase rather than with concentrations in the sediment. Even when shrimp, clams, and oysters were contaminated by oil exposures under field conditions rather than under laboratory conditions, they rapidly depurated N, MN, and DMN compounds when placed in the laboratory in oil-free seawater. The highest concentrations of oil in the water beneath the oil slick of the shrimp ponds were not enough to explain the large shrimp mortalities. It is suggested that behavioral responses caused shrimp to contact the oil slick at night resulting in the accumulation of lethal oil doses.